JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES
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2026
·
IF 2.5
Zhen Yang,Huiying Li,Wei Zhao,Yingxia Yu,Yanling Lin,Jianxuan Liu,Xinghu Fan,Moyan Wang,Xin Teng,Zhikai Qiu
Objective Evaluation of the therapeutic effect of Tongfu Zhike Formula (TFZKF) on mice with cough variant asthma (CVA) and exploration of its mechanism of action in improving CVA. Methods The main chemical components of TFZKF were detected and analyzed using UHPLC-MS/MS. Network pharmacology was employed to investigate the potential targets of TFZKF in CVA. After grouping and drug administration, the number of coughs and cough latency were observed in CVA mice. White blood cell differential counts in BALF, serum levels of IgE, IL-4, IL-5, IL-13 and IFN-γ, as well as pathological changes in lung tissue were assessed. Western blot and RT-qPCR were used to analyze the protein expression levels and mRNA changes of TLR4, MyD88, and NF-κB in the lung tissue of CVA mice. Results A total of 495 chemical components were detected in TFZKF under both positive and negative ion modes. Network pharmacology analysis identified 199 potential targets related to TFZKF and CVA, and found close associations with the TLR4 and NF-κB signaling pathways. Animal experiments showed that, compared to the Model group, TFZKF significantly reduced the number of coughs, prolonged cough latency, decreased serum levels of IgE, IL-4, IL-5, and IL-13, reduced the total number of white blood cells, neutrophils, and eosinophils in BALF, alleviated inflammatory cell infiltration and fibrosis in lung tissue, and downregulated the protein and mRNA expression of TLR4, MyD88, and NF-κB. Conclusion The interaction within the TLR4/MyD88/NF-κB signaling pathway may be a potential key target for the treatment of cough variant asthma.
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Scientific Reports
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2026
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IF 4.9
Li Ruifang,Sun Yan,Feng Mingzhi,Kelsang Drolma,Cai Hanhui,Zhang Jun
Ulcerative colitis (UC) is a chronic disease characterized by intestinal inflammation, mucosal damage, and immune dysregulation. Current treatments are often inadequate, driving the search for alternatives with fewer side effects. Isoliquiritigenin (ISL), a flavonoid from licorice, has demonstrated anti-inflammatory effects, but its efficacy in UC remains uncertain. Male C57BL/6 mice were divided into six groups: Control, DSS model, low-, medium-, and high-dose ISL (25, 50, 100 mg/kg), and 5-aminosalicylic acid (5-ASA, 100 mg/kg). UC was induced by administering 3% DSS, followed by ISL or 5-ASA treatment. Disease activity index (DAI), histopathology, real-time PCR, Western blotting, immunohistochemistry, and 16 S rRNA sequencing were used to assess inflammation, intestinal barrier integrity, and gut microbiota (GM) composition. a Caco-2 cell-based model of UC was developed. After transfection to induce the overexpression of TLR4 and its adaptor protein MyD88, the cells were incubated with ISL. The effects of this intervention were evaluated by measuring the expression of inflammatory cytokines, tight junction-associated proteins, and components of the TLR4/MyD88 signaling pathway. ISL significantly alleviated DSS-induced UC symptoms, such as weight loss and colonic shortening. ISL reduced colonic mucosal damage and inflammatory cell infiltration, downregulated TLR4, MyD88, and phosphorylated NF-κB expression, and lowered TNF-α, IL-1β, and IL-6 levels. It also improved intestinal barrier function by upregulating ZO-1, Claudin-1, and Occludin expression. ISL modulated GM by increasing beneficial bacteria (Muribaculaceae) and reducing pathogenic bacteria (Escherichia-Shigella). Overexpression of TLR4 and MyD88 in the Caco-2 cell line abrogated the protective effects of ISL, as evidenced by increased expression of inflammatory cytokines and downregulated expression of tight junction proteins. Overall, these findings suggest ISL may protects against DSS-induced UC by suppressing the TLR4/MyD88/NF-κB pathway, enhancing intestinal barrier function, and modulating GM, supporting its potential as a therapeutic supplement for UC.
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FASEB JOURNAL
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2025
·Vol. 39
·期 5
·e70439
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IF 4.2
Yun Li,Site Yu,Jizhang Zeng,Situo Zhou,Xu Cui,Jie Zhou,Pihong Zhang
Excessive inflammation is a prominent issue in diabetic wounds, leading to delayed healing or amputation. Corilagin (Cori) is a natural polyphenolic compound with diverse pharmacological activities, particularly its anti-inflammatory properties. The aim of this study was to evaluate the anti-inflammatory effect of Cori on diabetic wounds and to explore the potential underlying mechanisms. The impact of Cori on wound healing was assessed in streptozotocin (STZ)-induced diabetic mice through morphological observation, histological staining, and gene expression analysis. Flow cytometry, qRT-PCR, western blot analysis, and RNA sequencing were conducted to elucidate the underlying mechanisms in RAW264.7 cells. The results demonstrated that Cori accelerated wound healing, inhibited excessive inflammation, and regulated macrophage polarization in diabetic mice. In Vitro, Cori decreased M1 polarization and inhibited the expression of pro-inflammatory mediators in RAW264.7 cells. Sequencing analysis revealed that Cori exerts anti-inflammatory effects on RAW 264.7 cells through multiple targeted mechanisms. Moreover, in LPS-induced macrophages, Cori dramatically decreased the activation of TLR4, MyD88, and NF-κB. Additionally, Cori enhanced M2 polarization by promoting fatty acid oxidation. In conclusion, the findings suggest that Cori modulates macrophage polarization through various targeted mechanisms, effectively suppressing inflammation and accelerating diabetic wound healing. Graphical Diabetic ulcers are common chronic wounds marked by excessive and persistent inflammation, imposing significant healthcare and economic burdens. Corilagin (Cori) was shown to accelerate wound healing in STZ-induced diabetic mice by modulating macrophage polarization and suppressing inflammation. In vitro, Cori inhibited M1 polarization and reduced the expression of pro-inflammatory mediators via the TLR4/MyD88/NF-κB pathway, while promoting M2 polarization by enhancing fatty acid oxidation. This study highlights Cori's potential as a therapeutic agent for diabetic wound management through its multi-targeted anti-inflammatory mechanisms.
研究领域:
药理学
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免疫学
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分子生物学
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糖尿病研究
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INTERNATIONAL JOURNAL OF PHARMACEUTICS
·
2022
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IF 6.51
Tengteng Yuan,Shujie Lv,Wei Zhang,Yanan Tang,Hong Chang,Zihan Hu,Liang Fang,Jiaojiao Du,Sifan Wu,Xinli Yang,Yangfu Guo,Ruihan Guo,Zongrui Ge,Lei Wang,Caiyun Zhang,Rulin Wang,Weidong Chen
Paeoniflorin (PF) has a certain therapeutic effect on cholestasis liver injury. To further improve the bioavailability of PF and play its pharmacological role in liver protection, PF-phospholipid complex micelles (PF-PLC micelles) were prepared based on our previous research on PF-PLC. The protective effects of PF and PF-PLC micelles on cholestasis liver injury induced by 17α-ethynylestradiol (EE) were compared, and the possible mechanisms were further explored. Herein, we showed that PF-PLC micelles effectively improved liver function, alleviated liver pathological damage, and localized infiltration of inflammatory cells. Mechanism studies indicated that PF-PLC micelles treatment could suppress the TLR4/MyD88/NF-κB pathway, and further reduce the levels of pro-inflammatory factors. Meanwhile, our experimental results demonstrated that the beneficial effect of PF-PLC micelles on EE-induced cholestasis may be achieved by the upregulation of nuclear receptors and metabolic enzymes (PXR/CAR/UGT1A1). All these results indicate that PF-PLC micelles have great potential in the treatment of cholestatic liver disease.
研究领域:
药理学
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肝病学
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分子生物学
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Pharmaceuticals
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2026
·Vol. 19
·期 2
·275
·
IF 5.7
Zhongnan Hu,Hui Liu,Weihua Wu,Tayyab Ali,Adam Junka,Farukh S. Sharopov,Xuan Zou,Shisong Fang,Yanfang Sun
Background: Influenza A virus is an acute respiratory virus that spreads quickly, affects a broad range of populations, and can lead to many complications and mortality.ArtemisiaL. species are widely used in traditional medicine, but their antiviral potential against H1N1 remains uncertain.Methodology: Network pharmacology and molecular docking were used to computationally explore their potential function in this domain, and to investigate how their invasion mechanisms and adsorption occur. UPLC-MS/MS analysis identified the main components of the extracts. The anti-H1N1 mechanism ofArtemisiaL. extracts was studied in vitro.Results: Network pharmacology identified 95 key targets betweenArtemisiaL. and IAV, with quercetin and luteolin as core active compounds. Molecular docking predicted strong binding affinities between these compounds and influenza virus proteins. UPLC-MS/MS analysis identified 75, 100, and 64 chemical components inACBE,AALE, andACTE, respectively, mainly flavonoids and terpenoids.ArtemisiaL. extracts exhibited both preventive and therapeutic effects against H1N1, reducing progeny virus NP mRNA and protein levels. In vitro experiments showed that higher concentrations of the extracts prevent virus attachment to MDCK cells by denaturing the HA protein. NA plays an essential role in progeny virus release. We found that a high concentration of ACTE can inhibit NA up to 85%, and ACBE showed a low inhibitory effect on NA.Conclusions: In terms of therapeutic effects,ArtemisiaL. extracts can regulate intracellular inflammatory factors via the TLR4/NF-κB/MyD88 signaling pathways and reduce the expression of IL-1β, IL-6, TNF-α, TLR4, NF-κB, p65, and MyD88 at the mRNA level, thereby inhibiting H1N1 virus replication. These results suggest that bioactive components inArtemisiaL. extracts may inhibit H1N1, potentially leading to the development of natural-product-based anti-influenza agents.
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BMC GASTROENTEROLOGY
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2025
·Vol. 25
·期 1
·1-14
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IF 2.6
Yuan Zuohui,Yang Xiaoping,Wang Xiaochun,Shi Xinlong,Chen Jia,Huang Lijun,Yang Jie,Shi Yuping,Zhang Liping,Mai Ping
Section
Background
This study aimed to investigate the effects of melatonin on diarrhea and visceral hypersensitivity in rats with diarrhea-predominant irritable bowel syndrome (IBS-D) and to explore its potential mechanisms through modulation of the TLR4/MyD88/NF-κB pathway.
Section
Methods
Adult male Sprague-Dawley (SD) rats were used to establish an IBS-D model through a combination of chronic and acute stress. The rats were randomly divided into four groups: healthy control (HC), IBS-D, IBS-D + melatonin 5 mg/kg (M-L), and IBS-D + melatonin 10 mg/kg (M-H), with six rats in each group. Visceral sensitivity was assessed using the abdominal withdrawal reflex (AWR). The expression levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in colon tissue were measured using enzyme-linked immunosorbent assay (ELISA). Western blotting and immunohistochemistry were employed to detect the expression of TLR4, MyD88, and NF-κB proteins in colon tissue. Additionally, 16 S rRNA sequencing was used to analyze the composition of the intestinal microbiota.
Section
Results
Compared to the HC group, the IBS-D group exhibited colonic inflammatory injury, increased AWR scores, elevated levels of TNF-α, IL-6, TLR4, MyD88, and NF-κB in the colon, and altered intestinal microbiota composition. Melatonin treatment reduced colonic inflammatory injury, decreased AWR scores, and lowered the levels of TNF-α, IL-6, TLR4, MyD88, and NF-κB in a dose-dependent manner. The intestinal microbiota composition in melatonin-treated groups showed a trend towards that of the HC group.
Section
Conclusion
Melatonin improved diarrhea and visceral hypersensitivity in IBS-D rats, potentially through the modulation of the TLR4/MyD88/NF-κB pathway and partial restoration of the intestinal microbiota.
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Food & Function
·
2024
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IF 5.1
Bufan Xu,Luyao Zhang,Di Wu,Zihe Qi,Juanjuan Cao,Wenrui Li,Lihua Fan,Yiheng Shi,Yongning Wu,Guoliang Li
Copper II oxide nanoparticles (CuO NPs), a kind of widely used nanomaterial, have been detected in food and the environment, which has aroused widespread public concern. Recently, increasing data have suggested that intestinal microecology is closely related to immune homeostasis. However, the intestinal immunotoxicity induced by CuO NPs through intestinal microbiota is still unknown. Therefore, in this study, zebrafish were exposed to CuO NPs to explore intestinal immunotoxicity by evaluating physiological indicators, intestinal tissue injury, antioxidant enzyme activities, gene expression of immune factors, and changes in intestinal microbiota and its metabolites (short-chain fatty acids (SCFAs) and lipopolysaccharides (LPS)). The results revealed that the intestinal immunotoxicity of CuO NPs was mediated by the impact on intestinal microbiota and its metabolite levels. Specifically, changes were observed in the abundance of microbes that participated in the metabolism of SCFAs and LPS. The reduction in acetic acid, propionic acid and valeric acid upregulated GPR84 expression, and the decline in LPS levels further resulted in the suppression of the key immune regulatory pathways TLR4/MyD88/NF-κB, ultimately leading to intestinal immunotoxicity. This study would provide a scientific basis for the risk assessment of CuO NPs and a new perspective for research on the immunotoxicity of nanoparticles.
研究领域:
环境科学
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毒理学
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微生物学
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免疫学
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水生生物学
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FOOD AND CHEMICAL TOXICOLOGY
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2022
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IF 5.572
Dan Su,Aitong Lei,Chunchao Nie,Yi Chen
The potential mechanism for the protective effect of Ganoderma atrum ( G. atrum ) polysaccharide (PSG-1) on acrylamide (AA) induced intestinal damage in mice was explored. Results showed that PSG-1 pretreatment prevented AA-induced injury by decreasing intestinal permeability and serum D-lactate acid (D-Lac) levels and increasing the number of small intestinal goblet cells and IgA secreting cells. In addition, PSG-1 pretreatment effectively reduced malondialdehyde (MDA) level and raised superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) activities in the intestine. Furthermore, PSG-1 administration decreased the levels of pro-inflammatory factors including IL-1β, TNF-α, and IL-6, while the anti-inflammatory factor IL-10 was elevated. Meanwhile, PSG-1 could increase the performance of tight junction (TJ) proteins such as Occludin , Claudin-1 and ZO-1. Moreover, according to the isobaric tag for relative and absolute quantitation (iTRAQ) and Western blot results, PSG-1 could reduce AA-induced intestinal injury through TLR4/MyD88/NF-κB signaling pathway. Overall, the present study suggested that PSG-1 protected intestinal permeability and barrier function in mice via reducing inflammation and oxidative stress , and effectively prevented AA-induced intestinal injury in mice.
研究领域:
药理学
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免疫学
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分子生物学
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毒理学
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高影响因子
Frontiers in Nutrition
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2022
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IF 6.59
Qianqian Yao,Linlin Fan,Nan Zheng,Christophe Blecker,Véronique Delcenserie,Huiying Li,Jiaqi Wang
Gut microbiota dysbiosis, together with goblet cells dysfunction has been observed in ulcerative colitis cases. This study aims to evaluate the potential of 2′-fucosyllactose (2′-FL) supplementation in inhibiting intestinal inflammation through regulating gut microbiota, protecting goblet cells, and stimulating mucin secretion. 2′-FL was orally administered to C57BL/6J mice daily (400 mg/kg bw) for 21 days and 5% dextran sulfate sodium (DSS) was used to induce the colitis in the last 7 days. Meanwhile, fecal microbiota transplantation (FMT) was conducted to test the roles of gut microbiota in the remission of colitis by 2′-FL. Gut microbiota alteration was analyzed through 16S ribosomal RNA (16S rRNA) sequencing. Periodic acid-Schiff (PAS), immunofluorescence staining, as well as mucin 2 (MUC2) and NOD-like receptor family pyrin domain containing 6 (NLRP6) messenger RNA (mRNA) expression in colon fragments was performed and detected. The results showed that the DSS + 2′-FL mice were found to have a slower rate of weight loss, lower disease activity index (DAI) scores, and longer colon lengths than the DSS group ( p < 0.05), so in the FMT recipient mice which received fecal microbiota from the DSS + 2′-FL group. In addition, the data revealed that 2′-FL relieved the disorder of DSS-induced gut microbiota, including decreasing the high abundance of mucin-utilizing bacteria in the DSS group, such as Bacteroides, Lachnospiraceae NK4A136, Lachnospiraceae , and Bacteroides vulgatus . PAS and immunofluorescence staining showed that 2′-FL treatment promoted the recovery of goblet cells and enhanced MUC2 and NLRP6 expression, which was also observed in the FM (DSS + 2′-FL) group. Moreover, NLRP6, which has been proved to be a negative regulator for Toll-like receptor 4/myeloid differential protein-8/nuclear factor-kappa B (TLR4/MyD88/NF-κB) pathway, was upregulated by 2′-FL in colon tissue. In conclusion, this study suggests that 2′-FL ameliorates colitis in a gut microbiota-dependent manner. The underlying protective mechanism associates with the recovery of goblet cells number and improves MUC2 secretion through TLR4-related pathway.
研究领域:
免疫学
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微生物学
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胃肠病学
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分子生物学
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FOOD CHEMISTRY
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2022
·
IF 9.231
Chuang Liu,Zhichang Qiu,Duanyin Gu,Fangzhou Wang,Rentang Zhang
This study explored the structural characteristics of the purified blackened polysaccharide fraction (BJP-4) and its potential to alleviate colitis. BJP-4 had a molecular weight of 1.24 × 10 5 Da and mainly consisted of → 4)- α - l -Gal p A (1→, →5)- α - l -Ara f (1 → and → 4)- β - d -Gal p (1 → residues. After the administration of BJP-4, the disease activity index of colitic mice was reduced by 40.38–50.96%, accompanied by increased colon length (30.00–62.50%) and ameliorated pathological damage. The mechanisms involved regulation of the intestinal microbiota and subsequent inhibition of the TLR4/MyD88/NF- κ B/NLRP3 pathway, balance of pro/anti-inflammatory cytokines and oxidative status, enhancement of epithelial barrier integrity and production of short-chain fatty acids. In particular, high-doses of BJP-4 significantly increased the abundance of beneficial bacteria (f_ Muribaculaceae , Lactobacillus and Lachnospiraceae _NK4A136_group, 0.78–1.04-fold) and suppressed the levels of harmful bacteria (o_ Clostridia _UCG-014, Bacteroides and Escherichia-Shigella , 32.30–90.42%). These findings revealed the anti-inflammatory effects and mechanisms of purified blackened polysaccharides, which facilitated their application in functional foods.
研究领域:
药理学
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免疫学
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微生物学
·
营养学
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高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
·
IF 8.5
Xialin Sun,Tingwen Zhang,Yan Zhao,Han Yang,Yawei Li,Xin Sun,Xingbo Bian
Background Ulcerative colitis (UC) involves intestinal barrier dysfunction, immune dysregulation, and microbiota imbalance. Bletilla striata polysaccharide (BSP) shows anti-inflammatory potential, but its UC mechanisms remain unclear. Purpose To purify Bletilla striata polysaccharide (BSP-1), characterize its structure, and elucidate its multi-target UC therapeutic mechanisms. Methods This study purified a novel structure of neutral glucomannan with a small amount of acetylation (BSP-1). Together with tight junction protein analysis, oxidative stress markers, 16S rRNA sequencing, cytokine quantification, and molecular ecological network examination, the team used a UC mouse model created using dextran sodium sulfate (DSS). Results BSP-1 alleviated colitis by inhibiting TLR4/MyD88/NF-κB signaling (elevating IL-10; lowering IL-6, TNF-α, and IL-1β) and restoring integrity of the intestinal barrier via upregulating Occludin, ZO-1, MUC2, and Claudin-1. It reduced oxidative stress (lower MDA; higher SOD) and modulated gut microbiota (enriched Lactobacillus , suppressed Escherichia - Shigella ). Molecular ecological network analysis showed that BSP-1 restored microbial community stability by enhancing bacterial competition. Conclusion BSP-1 exerts integrated anti-inflammatory, barrier-repairing, and microbiota-regulating effects, highlighting its potential as a multi-target UC therapy and intestinal microecological regulator.
研究领域:
药理学
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免疫学
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微生物学
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分子生物学
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胃肠病学
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植物学
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生物化学
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SCIENCE OF THE TOTAL ENVIRONMENT
·
2021
·
IF 7.963
Weike Shaoyong,Wanrong Zhang,Chenyang Wang,Zhongyun Kou,Wenlong Yong,Junheng Jiao,Wenyong Yan,Weijun Pang
Decabromodiphenyl ether (BDE-209), a congener of polybrominated diphenyl ethers (PBDEs), is used as a flame retardant and accounts for over 82% of total PBDE usage. BDE-209 has been found to be persistent in indoor and outdoor environments and has adverse health effects on humans. This study aimed to investigate the effects of BDE-209 on mouse intestinal tissues and reveal the underlying toxicological mechanisms. In this study, C57BL/6J male mice were administered BDE-209 intragastrically (200 mg/kg bodyweight) once a day for 4 weeks, after which intestinal tissues, blood samples, and fecal samples were collected for analysis. The results showed that BDE-209 exposure significantly decreased body weight ( P < 0.01) and promoted intestinal oxidative stress, apoptosis, autophagy, and inflammation. Additionally, BDE-209 reduced the intestinal mucus barrier and increased gut permeability. Importantly, BDE-209 decreased the levels of intestinal short-chain fatty acids (SCFAs), including acetic acid ( P < 0.05) and butyric acid ( P < 0.01), which protect gut health. Mechanistically, BDE-209 triggered apoptosis by damaging mitochondrial function, increasing both the release of mitochondrial cytochrome c (Cyt c) into the cytosol and the Bax/Bcl-2 ratio, as well as inducing activation of caspase-3, caspase-9, and PARP. Moreover, BDE-209 exposure induced intestinal inflammation via the TLR4/MyD88/NF-κB signaling pathway and promoted intestinal autophagy by upregulating Beclin 1, leading to the accumulation of LC3-I to LC3-II. Therapeutically, N -acetyl-L-cysteine (NAC) attenuated the effects of BDE-209 on gut toxicity, including intestinal permeability, apoptosis, and inflammation through the oxidative stress pathway. Overall, we suggest that BDE-209 causes gut toxicity by modulating the intestinal barrier, permeability, oxidative stress, autophagy, apoptosis, and inflammation, and BDE-209 exposure could be partly reversed by antioxidant NAC supplementation. Our findings provide new insights into the intestinal response to BDE-209 exposure.
研究领域:
毒理学
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药理学
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分子生物学
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环境科学
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高影响因子
危险品化学品经营许可证（带存储）